Heterologous prime-boost regimen elicits potent humoral and cell-mediated immune responses and provides complete protection against SFTSV

Author:

Kim Jae-Yong1,Jeon Kyeongseok2,Hong Jung Joo3,Park Sang-In4,Cho Hyeong-Gon5,Park Hyo-Jung1,Kwak Hye Won4,Park Hyeong-Jun1,Bang Yoo-Jin1,Lee Yu-Sun1,Bae Seo-Hyeon1,Kim So-Hee2,Hwang Kyung-Ah6,Jung Dae-Im7,Cho Seong Hoo7,Seo Sang Hwan7,Kim Green3,Oh Hanseul3,Lee Hwal-Yong3,Kim Ki Hyun2,Lim Hee-Young8,Jeon Pyeonghwa8,Lee Joo-Yeon8,Chung Junho2,Lee Sang-Myeong9,Ko Hae Li10,Song Manki7,Cho Nam-Hyuk2,Lee Young-suk5,Hong So-Hee11,Nam Jae-Hwan1

Affiliation:

1. The Catholic University of Korea

2. Seoul National University College of Medicine

3. Korea Research Institute of Bioscience and Biotechnology

4. SML Biopharm

5. Korea Advanced Institute of Science and Technology (KAIST)

6. Genetree Research

7. International Vaccine Institute

8. National Institutes of Health, Korea Disease Control & Prevention Agency. Cheongju

9. Chungbuk National University

10. Scripps Korea Antibody Institute

11. Ewha Womans University

Abstract

Abstract Severe Fever with Thrombocytopenia Syndrome Virus(SFTSV) was first discovered in 2009 as the causative agent of severe fever with thrombocytopenia syndrome. Despite its potential threat to public health, no prophylactic vaccine is yet available. This study developed a heterologous prime-boost strategy comprising priming with recombinant replication-deficient human adenovirus type 5 (rAd5) expressing the surface glycoprotein, Gn, and boosting with Gn protein. This vaccination regimen induced balanced Th1/Th2 immune responses and resulted in potent humoral and T cell-mediated responses in mice. It elicited high neutralizing antibody titers in both mice and non-human primates. Transcriptome analysis revealed that rAd5 and Gn proteins induced adaptive and innate immune pathways, respectively. This study provides immunological and mechanistic insight into this heterologous regimen and paves the way for future strategies against emerging infectious diseases.

Publisher

Research Square Platform LLC

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